Although animal studies suggest that the benzodiazepine receptor complex mediates both the anxiolytic effects of these drugs and aspects of the anxiety state itself, no study has systematically examined the functional sensitivity of the benzodiazepine system in human anxiety states, mostly because of the difficulty in finding a reliable, quantitative measure of benzodiazepine effects. This study will test whether the reduction in saccadic eye movement velocity produced by the acute administration of multiple increasing doses of diazepam as compared with placebo, provides such a measure in patients with anxiety disorders by virtue of its correlation with the drug's sedative, amnestic, and anxiolytic effects; whether the sensitivity to benzodiazepines is decreased in both patients with panic disorder and generalized anxiety disorder compared with controls; and whether the degree of benzodiazepine sensitivity is related to severity of symptoms within each group. Other measures of benzodiazepine pharmacodynamics (i.e., the reductions in cortisol, ACTH, norepinephrine, epinephrine, memory and alertness) will be included to enhance group differentiation and provide a measure of effects at hypothetically different neuroanatomical loci. Confirmation of these findings will suggest that panic disorder and generalized anxiety disorder may share common neurobiologic substrates and not be as distinct as commonly thought. However, a comparison of the strength of separate biological-symptom severity correlations within the two groups may still provide support for some difference.